[ELEMENTS OF THE STUDY OF THE VESTIBULAR APPARATUS].
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Vertigo is uncommon in childhood. Its etiology is different from that of adults. Both central and peripheral disorders may give rise to vertigo symptoms in pediatric patients. The evaluation of vertigo in children requires a detailed history taking, clinical examination, audiometric assessment, and vestibular function tests. We present three pediatric patients with vertigo symptoms, together with treatment methods and results of treatment. Their ages ranged from 10 to 14 years. The diagnoses were vestibular neuritis in one patient, and benign paroxismal positional vertigo in two patients. Treatment was comprised of vestibular rehabilitation for vestibular neuritis, and canalith repositioning maneuver for benign paroxismal positional vertigo. All the patients benefited well from the procedures applied.
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Fifty-two patients receiving a cochlear implant were evaluated using vestibular function tests. Forty patients received an intracochlear implant. The risk of losing preoperative vestibular function is estimated to be around 50%. The authors suggest to implant with cochlear prosthesis the ear with preoperative decreased or total loss of vestibular function.
Children with a history of embryonic exposure to Accutane (isotretinoin) are at great risk for major physical malformations, brain malformations, and decreased intelligence. A case is presented of a 4-year 7-month-old black male with a history of embryonic exposure to Accutane who was born with embryopathy that includes bilateral major ear deformities. The child has a significant bilateral conductive hearing loss, and, in addition, a left sided sensorineural loss. Vestibular function testing revealed evidence of peripheral and central vestibular dysfunction. A course of diphenhydramine hydrochloride and Donnatal (phenobarbital, hyoscyamine sulfate, atropine sulfate, and scopolamine hydrobromide) significantly alleviated the symptoms of vestibular dysfunction. Otologic management of these children should include clinical documentation of the external deformities, evaluation of cochlear function, and early auditory habilitation. Vestibular function should also be evaluated in all children with a history of embryonic exposure to isotretinoin.
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The vestibulo-ocular reflex (VOR) is the only drive for short-latency eye movements stabilizing the retina during externally imposed, sudden, high-head accelerations. New strategies can exploit this unique VOR feature to study it under conditions relevant to the daily lives of patients, and to exclude the contributions from confounding nonvestibular mechanisms. Testing of the yaw vestibulo-ocular reflex (VOR) during random, whole-body rotational transients at < or = 2800 degrees/s2 delivered about centered and eccentric axes enables measurement of gains and millisecond latencies of the canal and otolith VORs in humans. Repeated measurements in acute unilateral deafferentation show sequential recovery of canal and otolith VORs to contralesional rotation, but severe and permanent deficits to ipsilesional rotation. Patients with bilateral loss of caloric responses show severe bilateral loss of VORs to transient rotation, suggesting that the apparent preservation of their VORs during sinusoidal rotations at moderate frequencies may be due instead to somatosensory inputs. Since visual acuity is degraded by retinal image motion, dynamic visual acuity (DVA) measured during imposed head-on-body or whole-body transient motion can correlate closely with VOR performance only if optotypes are presented during directionally and temporally unpredictable, high-acceleration head motion. Prediction and efference copy are relentlessly employed by vestibulopathic patients to enable good DVA during predictable or low-acceleration head motion. The linear VOR to transient lateral acceleration is strongly dependent upon viewing distance. The latency of this otolith VOR is slightly longer and more variable than the canal VOR. Unlike the canal VOR, the otolith VOR does not develop a strong directional asymmetry in unilateral deafferentation. The otolith VOR is bilaterally attenuated in bilateral vestibulopathy, and loses target distance dependence in cerebellar degeneration.